The aim of this research is to obtain basic information concerning how the bioenergetic apparatus and reactions in mammalian mitochondria change with the age of inbred golden hamsters on a "common" diet. These data will be rigorously compared with the results obtained under exactly the same conditions except the animal will be rationed with a high-fat and high-cholesterol diet. The survival curves or mortality rates for these two groups of hamsters will be also recorded with major classification of the causes of the deaths. More specifically, reliable growth charts and accurate mortality rates or survival curves of the hamsters on a "common" diet will be compared with similar data of hamsters on a "high-cholesterol and high- lipid" diet which contains an additional 25% saturated fat and 1.5% cholesterol. At 1.5 to 4 week intervals from new born to the death of all animals, we will study all bioenergetic components, the partial and complete electron tranport and energylinked reactions, such as States 3 and 4 oxidation, respiratory control, ADP/O ratio, ATPase, the activities of cytochrome oxidase, and NADH- and succinate-cytochrome c reductases, etc. The mitochondria of aorta, brain, heart, kidney and liver will be used. The effect of aging on the number or size of mitochondria, if any, will be studied by the determination of the per cent of mitochondrial protein per total tissue protein. When the focal points due to aging and/or diet are narrowed down or located, we will endeavor an in-depth study to find out "why". Our premise is that aging can be affected by dietary intake and old age or senescence may be considered a metabolic disease. Rejuvenation may be accomplished clinically and prevented effectively. Our rationale is that in order to achieve this goal to meet increasing demands for older people in the next century because of the changing trends of population growth and socio-economic systems, the cause of so-called senescence must be first uncovered and then remedied.